Key result
TGF-beta signaling regulates endothelial-mesenchymal transition, contributing to the formation of cardiac fibroblasts and the development of cardiac fibrosis.
Design
Review
Authors
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May identify TGF-β/EndMT as antifibrotic targets in HF; leaves open clinical validation of inhibitors.
Understanding the mechanisms of cardiac fibroblast formation via EndMT and TGF-β signaling may provide new therapeutic targets for heart diseases associated with fibrosis.
Yoshimatsu et al. (2011) conducted a review in Cardiac fibrosis. TGF-beta signaling was evaluated. TGF-beta signaling regulates endothelial-mesenchymal transition, contributing to the formation of cardiac fibroblasts and the development of cardiac fibrosis.
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